Denervation and the immune response in mice infected with Trypanosoma cruzi.
C57B1 mice were infected with Trypanosoma cruzi Y strain trypomastigotes and showed a peak of parasitaemia 9 days after infection. Virtually all mice survived the acute stage of infection and were aparasitaemic thereafter. Coincident with the peak of parasitaemia, there  was a progressive loss of cardiac neurones (up to  the 20th day after infection) and an appearance of T. cruzi antigen on myofibres. Anti-parasite immunity, evidenced by a significant inhibition of macrophage migration in the presence of T. cruzi  antigens (MIF test) and the deposition of complement and immunoglobulin in vivo around the nests of parasites, developed between days 7-10 after infection. Immunity to "self' components (MIF) test using neurone and heart antigens) was not detected until 15-20 days after infection. Although the MIF test detected a progressive increase in anti-neurone immunity between 20-90 days after infection, there was no additional loss of cardiac neurones during this period. In contrast to current hypotheses, these data suggest that the immunity to heart and neuronal antigens commonly detected in animals infected with T. cruzi is the result rather than the cause, of host cell destruction.
D000818:Animals; D000941:Antigens / Q000032:analysis; D002452:Cell Count; D002464:Cell Migration Inhibition; D014355:Chagas Disease / Q000276:immunology*; D003714:Denervation; D006321:Heart / Q000294:innervation*; D008214:Lymphocytes / Q000276:immunology; D008264:Macrophages / Q000276:immunology*; D051379:Mice; D008810:Mice, Inbred C57BL; D009474:Neurons / Q000276:immunology; D013997:Time Factors; D014349:Trypanosoma cruzi / Q000276:immunology
D000941:Antigens